Shock: Principles of Management

Chapter 77 Shock: Principles of Management



Thomas A. Santora, MD, Dipin Gupta, MD




Cases Considered



1. Shock following gunshot wound to the chest in a 21-year-old male

2. Shock following a motorcycle crash in a 33-year-old male

3. Shock following strenuous exercise in a 57-year-old male

4. An elderly female with mental status changes



Speaking Intelligently


When I’m asked to evaluate a critically ill patient, I always consider the processes that may cause rapid deterioration first—shock physiology is high on that list. If shock is present, the hx of events leading to the patient’s presentation will often provide insight into the underlying cause. When considering empiric resuscitation, I find it critical to determine if intrinsic cardiac dysfunction is the cause of the shock state, because all other causes of shock are initially treated with volume expansion.



Clinical Thinking


Questions I ask when caring for a patient in the ICU:


• Is shock physiology present in this patient?

• What is the probable classification (etiology) of this shock state?

• What interventions are needed to resuscitate (reverse) this hemodynamic abnormality?

• Will invasive hemodynamic monitoring help in the dx of this shock state? In the management of the shock state?

Shock is a sudden alteration in circulatory homeostasis that results in reduced perfusion of nutrients to organs and the cells thereof. Since living cells require a constant supply of nutrients for ongoing energy production to carry out their respective functions, when the necessary precursors (primarily oxygen) to fuel cellular energy production are not available to the cell, the less efficient anaerobic energy production pathway is used by cells with the production of reduced cellular energy and its end product, lactic acid. If the disruption of perfusion is severe or protracted, even the inefficient anaerobic energy production ceases and the cells lack the ability to produce the energy needed to maintain life-preserving functions. Shock physiology is recognized by the organ compromise that results from reduced cellular function within the respective organ.


The earliest and most common VS abnormality is tachycardia. This finding is nonspecific. Hypotension, generally considered systolic BP less than 90 mmHg, occurs late in the course of the shock state (following 30%–40% blood loss in hemorrhagic conditions; see the ATLS reference for more information). The clinician must be aware of the limitations of VS alone as a monitoring strategy for shock state surveillance. As cellular energy production becomes more dependent on the anaerobic pathway, the production of lactic acid increases, resulting in a measurable base deficit and decreased bicarbonate. Assessing these parameters may allow confirmation of a shock state.




Case 1


A 21-year-old male is brought to your ED with a gunshot wound to the left chest. Initial VS: BP 110/90, HR 124, RR 28. Your examination shows an agitated, uncooperative male with alcohol on his breath, a small bullet wound of the left chest at the third intercostal space mid-clavicular line, decreased breath sounds on the left, tracheal deviation to the right, and distended jugular veins.



Working Dx


This patient is in shock! He is manifesting this shock state (organ hypoperfusion) by agitation and lack of cooperation (CNS) and VS abnormality (increased HR, RR). Late recognition of shock physiology can result in a dead patient!


Critical Care Caveat: Consider the processes that can kill your patient the fastest and evaluate for them first! The CNS effect of alcohol can be a confounding factor; you must evaluate/eliminate the possibility of shock before attributing the above signs to intoxication.




Medical Knowledge


The etiology of shock can be classified as an abnormality of one of the three basic components of the circulation. The circulation consists of a pump (heart), the conduits (vessels), and the blood (intravascular volume). Classification systems have been devised to provide insight into the underlying causative process or to describe the appearance of the patient on clinical examination (cold vs. warm extremities). Hemorrhagic or hypovolemic shock states result from loss of intravascular volume. Cardiogenic shock results from intrinsic myocardial dysfunction, either ischemic (MI) or nonischemic, or from a functional impairment of the heart due to obstruction of venous return. In vasodilatory shock, dysfunction of the vessels results in impaired distribution of blood to the organs. The vasodilatation results from lack of normal sympathetic tone in neurogenic shock, release of bradykinins and histamines in anaphylactic shock, and an overwhelming cascade of vasoactive cytokines in septic shock. Knowledge of the hx predating the acute events will provide insight into the potential causes of the shock state.



















Cold Shock Warm Shock
Hemorrhagic, hypovolemia Septic
Cardiogenic Neurogenic

image Intrinsic myocardial
  

image Extrinsic (restrictive)
image Tamponade

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Mar 20, 2017 | Posted by in GENERAL SURGERY | Comments Off on Shock: Principles of Management

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